Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) regulates growth and patterning of the postnatal mouse cerebellum

Kim, Bum Joon; Takamoto, Norio; Yan, Jun; Tsai, Sophia Y.; Tsai, Ming‐Jer

doi:10.1016/j.ydbio.2008.11.001

Cited by 48 publications

(45 citation statements)

References 56 publications

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“…In SF1-COUP-TFII mice hypothalami, none of the described COUP-TFII target genes such as γ-aminobutyric acid type A receptor alpha 1 (GABAA-R α1), carnitine palmitoyltransferase I (CPT-1), or insulin-like growth factor 1 were affected (17,29,30) (Fig. S5).…”

Section: Sf1-coup-tfii Mice Present Hypothalamic Hypersensitivity To mentioning

confidence: 99%

Hypothalamic ventromedial COUP-TFII protects against hypoglycemia-associated autonomic failure

Sabra-Makke

Maritan

Planchais

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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The nuclear receptor Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) is an important coordinator of glucose homeostasis through its function in different organs such as the endocrine pancreas, adipose tissue, skeletal muscle, and liver. Recently we have demonstrated that COUP-TFII expression in the hypothalamus is restricted to a subpopulation of neurons expressing the steroidogenic factor 1 transcription factor, known to play a crucial role in glucose homeostasis. To understand the functional significance of COUP-TFII expression in the steroidogenic factor 1 neurons, we generated hypothalamic ventromedial nucleus-specific COUP-TFII KO mice using the cyclization recombination/locus of XoverP1 technology. The heterozygous mutant mice display insulin hypersensitivity and a leaner phenotype associated with increased energy expenditure and similar food intake. These mutant mice also present a defective counterregulation to hypoglycemia with altered glucagon secretion. Moreover, the mutant mice are more likely to develop hypoglycemia-associated autonomic failure in response to recurrent hypoglycemic or glucopenic events. Therefore, COUP-TFII expression levels in the ventromedial nucleus are keys in the ability to resist the onset of hypoglycemia-associated autonomic failure.H ypothalamic neurons are able to detect changes in the concentration of circulating hormones and nutrients and to relay this information into adaptive signals toward peripheral organs aimed at maintaining glucose homeostasis and energy balance. Among these neurons, several studies have shown that the steroidogenic factor 1 (SF1) expressing ones, which are restricted to the hypothalamic ventromedial nucleus (VMN), are important modulators of metabolic functions through their ability to detect variations of extracellular concentrations of glucose, insulin, leptin, and orexin to coordinate insulin/glucose homeostasis (1-5). The SF1 transcription factor itself is a key actor of energy homeostasis ,as SF1 knockout (KO) mice are obese (6). SF1 KO mice display an abnormal organization of the VMN, as SF1 is necessary for the terminal differentiation of the VMN neurons (7,8). SF1 itself directs a genetic program involved in energy homeostasis and leptin action in the VMN (9). Outside these functions, SF1 neurons are also part of the neurocircuitry involved in the counterregulatory response (CRR) to hypoglycemia. To prevent hypoglycemia, organisms have developed several survival mechanisms of CRR such as decreased insulin secretion and increased glucagon secretion to quickly reestablish euglycemia (10, 11). The decreased insulin secretion is a direct effect of hypoglycemia on the pancreatic β cells, while the other CRRs are mainly directed by the central nervous system and in part by the SF1 neurons (12)(13)(14). Overall the SF1 neuronal population is at the interface between sensing of glucose concentrations and modulation of insulin-dependent metabolism and energy homeostasis.Recently we have observed that Chicken Ovalbumin Upstre...

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Section: Sf1-coup-tfii Mice Present Hypothalamic Hypersensitivity To mentioning

confidence: 99%

Hypothalamic ventromedial COUP-TFII protects against hypoglycemia-associated autonomic failure

Sabra-Makke

Maritan

Planchais

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…Our laboratories have previously demonstrated that COUP-TFII acts as a positive regulator, enhancing target gene expression by interacting with Sp1 at Sp1-binding sites (Kim et al, 2009;Lin et al, 2010;Pipaon et al, 1999;Qin et al, 2010). To assess whether COUP-TFII regulates Eya1 expression through its interaction with Sp1, we searched for the evolutionarily conserved Sp1-binding sites in human, mouse and rat sequences on and surrounding the Eya1 gene and found three conserved sites upstream of the transcription start site (Fig.…”

Section: Coup-tfii Directly Regulates Eya1 Gene Expression By Interacmentioning

confidence: 99%

“…Although biochemical studies indicate that these two factors have similar DNA-binding and transcriptional activity in vitro, the patterns of COUP-TFI and COUP-TFII expression are distinct from each other. COUP-TFII is expressed in the mesenchyme of developing organs and is shown to play a key role in their organogenesis, cell fate determination, cell differentiation, angiogenesis and metabolic homeostasis (Kim et al, 2009;Kurihara et al, 2007;Li et al, 2009;Lin et al, 2010;Qin et al, 2008;Tang et al, 2010;Xie et al, 2011;You et al, 2005a;You et al, 2005b). During kidney development, COUP-TFII expression is detectable in the condensed mesenchyme and Human embryonic kidney 293 (HEK 293) cells were transfected with Lipofectamine 2000 (Invitrogen) according to the manufacturer's protocol.…”

Section: Introductionmentioning

confidence: 99%

COUP-TFII is essential for metanephric mesenchyme formation and kidney precursor cell survival

Tang

Suh

et al. 2012

Development

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SUMMARYDevelopment of the metanephric kidney in mammals requires complex reciprocal tissue interactions between the ureteric epithelium and the mesenchyme. It is believed that Gdnf, produced in the metanephric mesenchyme, activates Ret signaling in the Wolffian duct to initiate the formation of the metanephros. However, the molecular mechanism for induction of Gdnf in the metanephric mesenchyme is not completely defined. Previous studies demonstrated that during the early stages of kidney development, loss of Osr1, Eya1, Pax2 or Wt1 gene function in the metanephric mesenchyme compromises the formation of the kidney. Moreover, it has been shown that the Hox11-Eya1-Pax2 complex activates the expression of Six2 and Gdnf in the metanephric mesenchyme to drive nephrogenesis. Here, we demonstrate that the orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor II (COUP-TFII, also known as Nr2f2) is required for the specification of the metanephric mesenchyme. Deletion of COUP-TFII at E7.5 results in improper differentiation of the metanephric mesenchyme and absence of essential developmental regulators, such as Eya1, Six2, Pax2 and Gdnf. Importantly, we show that COUP-TFII directly regulates the expression of both Eya1 and Wt1 in the metanephric mesenchyme. Our findings reveal, for the first time, that COUP-TFII plays a central role in the specification of metanephric fate and in the maintenance of metanephric mesenchyme proliferation and survival by acting as a crucial regulator of Eya1 and Wt1 expression.

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“…These results suggest that COUP-TFs repress Pax6 transcription directly via binding to the DR1 element. COUP-TFI and COUP-TFII can also function indistinguishably as activators through protein-protein interaction with Sp1 transcription factors Park et al, 2002;Pipaon et al, 1999;Kim et al, 2009). The expression of Otx2 was decreased in both the double-mutant mouse and in COUP-TF-depleted ARPE-19 cells, revealing that COUP-TFI and COUP-TFII could positively regulate its expression.…”

Section: Research Articlementioning

confidence: 99%

COUP-TFs regulate eye development by controlling factors essential for optic vesicle morphogenesis

et al. 2010

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SUMMARYTranscriptional networks, which are initiated by secreted proteins, cooperate with each other to orchestrate eye development. The establishment of dorsal/ventral polarity, especially dorsal specification in the optic vesicle, is poorly understood at a molecular and cellular level. Here, we show that COUP-TFI (Nr2f1) and COUP-TFII (Nr2f2) are highly expressed in the progenitor cells in the developing murine eye. Phenotype analysis of COUP-TFI and COUP-TFII single-gene conditional knockout mouse models suggests that COUP-TFs compensate for each other to maintain morphogenesis of the eye. However, in eye-specific COUP-TFI/TFII doubleknockout mice, progenitor cells at the dorso-distal optic vesicle fail to differentiate appropriately, causing the retinal pigmented epithelium cells to adopt a neural retina fate and abnormal differentiation of the dorsal optic stalk; the development of proximoventral identities, neural retina and ventral optic stalk is also compromised. These cellular defects in turn lead to congenital ocular colobomata and microphthalmia. Immunohistochemical and in situ hybridization assays reveal that the expression of several regulatory genes essential for early optic vesicle development, including Pax6, Otx2, Mitf, Pax2 and Vax1/2, is altered in the corresponding compartments of the mutant eye. Using ChIP assay, siRNA treatment and transient transfection in ARPE-19 cells in vitro, we demonstrate that Pax6 and Otx2 are directly regulated by COUP-TFs. Taken together, our findings reveal novel and distinct cell-intrinsic mechanisms mediated by COUP-TF genes to direct the specification and differentiation of progenitor cells, and that COUP-TFs are crucial for dorsalization of the eye.

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Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) regulates growth and patterning of the postnatal mouse cerebellum

Cited by 48 publications

References 56 publications

Hypothalamic ventromedial COUP-TFII protects against hypoglycemia-associated autonomic failure

Hypothalamic ventromedial COUP-TFII protects against hypoglycemia-associated autonomic failure

COUP-TFII is essential for metanephric mesenchyme formation and kidney precursor cell survival

COUP-TFs regulate eye development by controlling factors essential for optic vesicle morphogenesis

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